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Deletion of Metal Transporter Zip14 (Slc39a14) Reduces Major Histocompatibility Complex II Expression in Murine Small Intestinal Epithelial Cells

ABSTRACT: Deletion of Metal Transporter Zip14 (Slc39a14) Reduces Major Histocompatibility Complex II Expression in Murine Small Intestinal Epithelial Cells

PROVIDER: PRJNA1179338 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31146203_1.fastq.gz	Fastqsanger.gz
	SRR31146203_2.fastq.gz	Fastqsanger.gz
	SRR31146204_1.fastq.gz	Fastqsanger.gz
	SRR31146204_2.fastq.gz	Fastqsanger.gz
	SRR31146205_1.fastq.gz	Fastqsanger.gz

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Deletion of Metal Transporter Zip14 (Slc39a14) Reduces Major Histocompatibility Complex II Expression in Murine Small Intestinal Epithelial Cells

Project description:Documented worldwide, impaired immunity is a cardinal signature resulting from loss of dietary zinc, an essential micronutrient. A steady supply of zinc to meet cellular requirements is regulated by an array of zinc transporters. Deletion of the transporter Zip14 (Slc39a14) in mice produced intestinal inflammation. Elevated fecal lipocalin-2, calprotectin, IgG levels and dysbiosis support the inflammatory phenotype. Here we show through RNA-sequencing, using purified intestinal epithelial cells (IECs), that Zip14 deletion produces markedly reduced expression of major histocompatibility complex class II (MHCII) molecules and the master MHCII trans-activator (Ciita). qPCR, western analysis and immunohistochemistry confirmed loss of MHCII. Spectrofluorimetry with zinc probe FluoZin-3 showed reduced labile zinc in IECs from knockout mice. Chromatin immunoprecipitation assays, using Ciita antibody and IEC chromatin, suggest decreased transcription accounts for depressed expression of specific MHCII genes. ATAC-sequencing (ATAC-seq) demonstrated that H2-Aa, H2-Ab1 and other MHCII genes result from chromatin remodeling yielding closed chromatin at regulatory regions of these genes. In agreement, ATAC-seq showed peak density of the chromosomal regulatory region of Ciita is consistent with down regulation of specific MHCII genes in IECs with Zip14 loss. Finally, dietary zinc supplementation of knockout mice and zinc supplementation of intestinal organoids in-vitro with Zip14 deletion restored transcript levels. Taken together, our data suggest that cellular zinc delivery, via Zip14, is necessary for proper chromatin occupancy, required for normal MHCII expression and effective immune functions, and to preclude inflammatory disorders of the small intestine.

2025-01-22 | GSE280523 | GEO

DNA methylation changes at major histocompatibility complex in multiple sclerosis

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Kinetics of abacavir-induced remodelling of the Major Histocompatibility Complex class I peptide repertoire

Project description:Characterisation of the kinetics of abacavir-induced perturbation of the immunopeptidome of the Major Histocompatibility Complex (MHC) class I molecule HLA-B*57:01.

2021-05-11 | PXD024331 | Pride

Hypomethylation mediates genetic association with the major histocompatibility complex genes in Sjögren's syndrome

Project description:Hypomethylation mediates genetic association with the major histocompatibility complex genes in Sjögren's syndrome

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DNA methylation changes at major histocompatibility complex in multiple sclerosis

Project description:The major histocompatibility complex (MHC) region represents by far the strongest multiple sclerosis (MS) susceptibility loci. DNA methylation changes have been consistently detected at the MHC region in MS. However, understanding the full picture of epigenetic regulations of MHC in MS remains challenging, due in part to the limited coverage in the region by standard whole genome bisulfite sequencing or array-based methods. To fill this gap, we utilized a novel but validated MHC capture protocol with bisulfite sequencing and conducted a comprehensive analysis of MHC methylation landscapes in blood samples from 147 treatment naïve MS participants and 129 healthy controls. We identified 132 differentially methylated region (DMRs) within MHC regions and found they are significantly overlapped with MS risk variants. Integration of the MHC methylome to human leukocyte antigen (HLA) genetic data further indicate that the methylation changes are significantly associated with HLA genotypes. Using DNA methylation quantitative trait loci (mQTL) mapping and the causal inference test (CIT), we identified 643 cis-mQTL-DMRs paired associations including 71 DMRs possibly mediating causal relationships between 55 SNPs and MS risk.

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Transcriptional down-regulation of major histocompatibility complex as a possible pathogenesis for Meniere's disease

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Transcription profiling of yeast expressing mouse major histocompatibility complex class I heavy chain H-2K(b)

Project description:To dissect the requirements of membrane protein degradation from the ER, we expressed the mouse major histocompatibility complex class I heavy chain H-2K(b) in yeast. Like other proteins degraded from the ER, unassembled H-2K(b) heavy chains are not transported to the Golgi but are degraded in a proteasome-dependent manner. The overexpression of H-2K(b) heavy chains induces the unfolded protein response (UPR). In yeast mutants unable to mount the UPR, H-2K(b) heavy chains are greatly stabilized. This defect in degradation is suppressed by the expression of the active form of Hac1p, the transcription factor that upregulates UPR-induced genes. These results indicate that induction of the UPR is required for the degradation of protein substrates from the ER.

2005-06-28 | E-SMDB-1576 | biostudies-arrayexpress

Enterocyte-specific deletion of metal transporter Zip14 (Slc39a14) alters intestinal homeostasis through epigenetic mechanisms

Project description:Enterocyte-specific deletion of metal transporter Zip14 (Slc39a14) alters intestinal homeostasis through epigenetic mechanisms

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Genetic variants in Major Histocompatibility Complex-linked genes Associate with Pediatric Liver Transplant Rejection

Project description:Limited access to large samples and independent replication cohorts precludes genome-wide association (GWA) studies of rare but complex traits. To localize candidate genes in an on-going study utilizing family-based GWA, a novel exploratory analysis was first tested on 1,774 major histocompatibility complex single nucleotide polymorphisms (SNPs) in 240 DNA samples from 80 children with primary liver transplantation (LTx), and their biological parents. Genotyping was performed using the Illumina HumHap550k SNP BeadArray; the genotype calls for the 1813 SNPs in the MHC region are provided in the genotype_data.zip supplementary file linked to this series (see README file in the zip archive for more information). The Affymetrix Human Exon 1.0 ST array was used to measure differential splicing patterns in archived RNA isolated from 26 of 80 children for genes found near associated SNPs. This SuperSeries is composed of the SubSeries listed below.

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RNA-seq analysis of the effect of kanamycin and the ABC transporter AtWBC19 on Arabidopsis thaliana seedlings reveals changes in metal content

Project description:Plants are exposed to antibiotics produced by soil microorganisms but little is known about their responses at the transcriptional level. Likewise, few endogenous mechanisms of antibiotic resistance have been reported. The Arabidopsis thaliana ATP Binding Cassette (ABC) transporter AtWBC19 (ABCG19) is known to confer kanamycin resistance, but the exact mechanism of resistance is not well understood. Here we examined the transcriptomes of control seedlings and wbc19 mutant seedlings using RNA-seq analysis. Exposure to kanamycin indicated changes in the organization of the photosynthetic apparatus, metabolic fluxes and metal uptake. Elemental analysis showed a 60% and 80% reduction of iron uptake in control and wbc19 mutant seedlings respectively, upon exposure to kanamycin. The drop in iron content was accompanied by the upregulation of the gene encoding for FERRIC REDUCTION OXIDASE 6 (FRO6) in mutant seedlings but not by the differential expression of other transport genes known to be induced by iron deficiency. In addition, wbc19 mutants displayed a distinct expression profile in the absence of kanamycin. Most notably, the expression of several zinc ion binding proteins, including ZINC TRANSPORTER 1 PRECURSOR (ZIP1), was increased, suggesting abnormal zinc uptake. Elemental analysis confirmed a 50% decrease of zinc content in wbc19 mutants. Thus, the antibiotic resistance gene WBC19 appears to also have a role in zinc uptake. Examination of transcriptome in control and wbc19 mutant seedlings with or without exposure to kanamycin.

2014-06-20 | E-GEOD-58662 | biostudies-arrayexpress

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